Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0022116 (ischemia)
 91,303 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Localized in vivo proton magnetic resonance spectra obtained from diseased areas in 2 patients with chronic localized encephalitis (Rasmussen's syndrome) showed reduced resonance intensities from N-acetyl compounds, suggesting focally decreased N-acetylaspartate concentrations. One of the patients had epilepsia partialis continua secondary to the encephalitis. In this patient, the spectra demonstrated a high lactate resonance intensity (not seen in the normal, contralateral hemisphere) corresponding to an estimated local concentration of about 7.5 mM. We speculate that the observed decrease in the N-acetyl compound resonance may be a biochemical correlate of the neuronal loss characteristic of this disease. The results establish that excessive accumulation of lactate can occur in the human brain as a result of seizure activity even in the absence of ischemia. Thus, bioenergetic compromise may be 1 predisposing factor to the death of excitable cells in the epileptogenic area.
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PMID:A proton magnetic resonance spectroscopy study of focal epilepsy in humans. 211 99

70 fetuses (10 to 37 weeks) and 30 full term infants were examined by ultrasound (U.S.). Anatomic correlations were made with frontal, axial and sagittal sections of 43 fetal and 3 neonatal brains. At 12 weeks gestational age (w.g.a.) only the inter hemispheric fissure is seen by U.S. The sylvian fissure (21 w.g.a.), the callosal sulcus (21 w.g.a.), the parieto-occipital sulcus (25 w.g.a.), the calcarine fissure (25 w.g.a.), the cingulate sulcus (26 w.g.a.) and the collateral sulcus (25-27 w.g.a.) are visualized rather late with in-utero U.S. The other sulci are more difficult to see. The peripheral location of these sulci contributes to the difficulty encountered in their visualization. The morphology of the sylvian fissure is quite characteristic on U.S. imaging and can be used to estimate the gestational age of the fetus. Compared to the embryological development there is a 2-4 weeks delay between the first infolding of the brain and the visualization of a sulcus by U.S. Abnormal sulcal patterns can be recognized based on the normal appearance for each gestational age. Sulcal anomalies are quite specific in holoprosencephaly, lissencephaly, micropolygyry, schizencephaly, agenesis of the corpus callosum. Silhouetting of the sulci may occur if the parenchymal echogenicity is sufficiently increased that the sulci no longer stand out (ischemia, tumors, encephalitis). Thickening of the sulci occurs in subdural hematomas, external hydrocephalus, meningitis and toxoplasmosis.
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PMID:[Echographic aspects of cerebral sulci in the ante- and perinatal period]. 305 86

Ten patients with encephalitis disseminata and 10 patients with cerebral ischemia underwent computed tomography and magnetic resonance imaging examinations. The results before and after the application of contrast media were compared. It is shown that T1-weighted MRI images, even after application of gadolinium-DTPA, are of little value for differential diagnosis of these diseases. In contrast, T2-weighted images did support the diagnosis of an acute stage of encephalitis disseminata versus acute ischemia. This was also true for lesions that had not been adequately depicted by computed tomography.
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PMID:Balance of T1-weighted images before and after application of a paramagnetic substance (Gd-DTPA). 345 67

Monitoring modalities unique to the neurologic intensive care unit include intracranial pressure monitors and neuroelectrophysiologic monitors. Each modality fullfills criteria for accuracy, responsivity during clinical change, and stability over time for trend analysis. Intracranial pressure monitoring may be accomplished by any of three approaches--ventricular catheter, subarachnoid bolt, or epidural pressure transducer. Intracranial pressure control has proved beneficial in at least three different illnesses--acute closed head injury, acute noncommunicating hydrocephalus, and Reye's syndrome. Other illnesses, such as cerebral hemorrhage, near drowning, meningitis, encephalitis, and cerebral mass lesions, are often associated with ICP elevations. Neuroelectrophysiologic monitoring encompassing electroencephalography (EEG), signal-processed EEG, and evoked potentials has proved to be most beneficial to the intensive care setting. Evoked potentials are most useful for monitoring patients in drug-induced coma or muscle paralysis in whom a clinical neurologic examination is unreliable. Focal neurologic deficits, incipient brainstem ischemia, and possibly brain death can be deduced from multimodality-evoked potentials (brainstem auditory and somatosensory). Evoked potential apparatus can be used to record sequential stimuli and trend changes. Signal-processed EEG apparatus (compressed spectral array and cerebral function monitor) are used to assess global or regional EEG activity for longer periods of time. Interpretation of signal-processed EEG recording requires some experience with this technique, but it is much easier to interpret than a standard 16-lead EEG. These monitors are useful in evaluating some forms of abnormal EEG activity and in monitoring gross changes in global or regional electrical activity. Currently available technology offers dynamic insight into the management of acute neurologic illnesses. The technology in evoked potential and signal processed EEG monitoring will eventually reduce the size and complexity of the instrumentation, making its application routine. Intracranial pressure monitoring is already routine in many intensive care units, although its use is occasionally sporadic. We believe that application of appropriate neurologic monitors improves therapy and outcome in neurologically injured and ill patients.
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PMID:Neurologic intensive care unit monitoring. 391 79

High dose barbiturates were used to treat intracranial hypertension in 15 patients with nontraumatic brain lesions; (3 hypertensive hemorrhage, 4 subarachnoid hemorrhage, 5 infarction, 2 global anoxia-ischemia and 2 encephalitis). All had persistently raised intracranial pressure (ICP) while being treated with aggressive conventional therapy. The addition of barbiturates caused an initial lowering of ICP in 11 patients, but only 5 of these had sustained ICP reductions. Survival of the 5 patients with persistently lowered ICP and death of the remaining 10 may indicate an improvement in outcome attributable to the addition of high dose barbiturates to conventional therapy in non-traumatic brain swelling. Because of the resources required for their prolonged use, randomized studied in patients with intracranial hypertension are required to determine the effect of barbiturates on outcome.
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PMID:High dose barbiturates in non-traumatic brain swelling: ICP reduction and effect on outcome. 714 92

We studied 53 patients (64% females) with static brain lesions who developed progressive movement disorders. Of these, 50 (94%) had dystonia, 17 (32%) tremor, eight (15%) parkinsonism, seven (13%) myoclonus, and three (6%) chorea. The precipitating insults included perinatal hypoxia/ischemia in 22 (42%), stroke in 12 (23%), head injury in eight (15%), encephalitis in eight (15%), and carbon monoxide poisoning, kernicterus, and radiation necrosis in one patient (2%) each. Among the 30 patients with initial insult occurring at age 2 years or younger (Infant group), distribution of dystonia at follow-up was focal in three (10%), segmental in eight (27%), unilateral in 10 (33%), and generalized in nine (30%). The mean latency between the original injury and onset of movement disorder was 25.5 +/- 16.7 years. Among the nine patients who developed dystonia after an insult occurring between ages 6 and 17 (Childhood group), the distribution of dystonia at follow-up was segmental in two (33%) and unilateral in seven (78%); the mean latency of dystonia onset was 4.9 +/- 7.8 years. Of the 14 patients in the Adult group (injury at age 25 or older), 11 developed dystonia, two developed parkinsonism, and one had carbon monoxide encephalopathy and parkinsonism. The distribution of dystonia in the 11 patients at follow-up was segmental in three (27%) and unilateral in eight (73%). The mean latency of movement disorder onset in the 14 patients of the Adult group was 2.5 +/- 4.9 years. No individuals in the Childhood or Adult groups became left-hand dominant; by comparison, nine of the 30 individuals in the Infant group became left-handed. In conclusion, brain injury at a young age is associated with a longer latency to onset of subsequent movement disorder, a greater tendency to development of generalized dystonia, and a greater probability of altered handedness. These tendencies may result from differences in age-related neuroplasticity.
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PMID:Delayed-onset progressive movement disorders after static brain lesions. 890 76

In order to identify the brain lesions of symptomatic/cryptogenic partial epilepsies (S/CPEs) in infants and children, magnetic resonance imaging (MRI) studies, thorough encephalographic (EEGic) studies, and detailed clinical and neurologic evaluations were obtained in 300 infants and children who were diagnosed to have S/CPEs with onset before the age of 13 years during the past 7 years. The overall detection rate of brain lesions by MRI was 41.7% (125/300). Congenital malformations (18 cases), vascular malformations (9 cases), neurocutaneous syndromes (13 cases), and space-taking lesions (20 cases) constitute a large percentage of SPEs in infants and children. A variety of insults such as infection, ischemia, hemorrhage, trauma and metabolic disorders can result in destructive parenchymal loss lesions including porencephaly, focal atrophy, hemiatrophy, and diffuse brain atrophy (20 cases). Major etiologic factors leading to infarction, encephalomalacia, leukomalacia, included trauma, hvpoxicischemic encephalopathy (HIE), systemic lupus erythematosus (SLE), encephalitis, vasculitis, venous thrombosis, vasculopathies, and heart problems (22 cases). Mesial temporal sclerosis (MTS) could be evidenced in around 20% (18/95) of cases with temporal lobe epilepsy (TLE), which was strongly associated with past histories of febrile seizures and encephalitis complicated by status epileptics. However, cases with porencephaly, global atrophy or delayed myelination of unilateral temporal lobe on MRI were more related to HIE. With the advent of neuroimaging techniques, particularly MRI, a wide variety of underlying pathology can be detected as a cause of symptomatic partial epilepsies in pediatric patients. The occurrence of S/CPE indicates the presence of localized brain dysfunction, and many of the causes are potentially treatable. An orderly and thorough clinical and laboratory investigations, as well as neuroimaging studies should be made to diagnose and treat any underlying conditions.
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PMID:Magnetic resonance imaging in symptomatic/cryptogenic partial epilepsies of infants and children. 915 66

Advanced paediatric ultrasound of the central nervous system (CNS) requires 7 MHz sector and linear transducers, equipment which is highly sensitive to flow velocity (Power Doppler) and additional transcranial axial, coronal and sagittal imaging. New diagnostic possibilities include recognition of subarachnoid hemorrhage (imaging of cisterns and/or CSF-flow); differentiation between subarachnoid and subdural fluid collections (colour flow imaging of traversing veins); additional criteria suggestive of spinal cord tethering (spinal cord pulsations); and grey-white matter differentiation in newborn infants. A meticulous examination technique is mandatory when investigating suspected brain death, sinus venous thrombosis, diffuse early ischemia or viral (herpes) encephalitis. Anatomical areas such as the cerebral aqueduct, tentorium, Foramina of Luschka or circle of Willis which are not usually regarded as accessible to cerebral echography can be visualized by advanced transcranial imaging technique. Indications for transcranial scanning; shortcomings of cerebral ultrasound; measures to overcome limitations; and requirements for present and future ultrasound equipment are given and discussed in tables.
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PMID:Advances in paediatric CNS ultrasound. 951 20

It is clear that inflammatory processes contribute to neurodegenerative disease, stroke, closed head injury, encephalitis, and other CNS disorders. These inflammatory processes are marked by local increases in cytokines, in particular tumor necrosis factor-alpha (TNF-alpha). It is important to control such CNS inflammation in order to preserve neural function. The neuroimmunomodulatory peptide alpha-melanocyte-stimulating hormone (alpha-MSH) has been shown to modulate peripheral inflammation by acting on melanocortin receptors in host cells (macrophages, neutrophils) to inhibit production of such proinflammatory agents. Our results indicate that alpha-MSH likewise acts directly within the brain to modulate local inflammation. To determine if microglia are involved in anti-inflammatory responses to alpha-MSH within the brain, murine cells were tested; they produced TNF-alpha and nitric oxide in response to challenge, and production of both was reduced by alpha-MSH. In tests on human astrocytes, both alpha-MSH (1-13) and alpha-MSH (11-13) reduced TNF-alpha. Ischemia/reperfusion in the posterior circulation in dogs causes inflammatory reactions and disturbance of function, estimated from decreases in auditory-evoked potentials. These deficits were reduced by administering alpha-MSH systemically during reperfusion, moreso when the peptide was given during both ischemia and reperfusion. The results indicate that, much as for inflammation in the periphery, alpha-MSH modulates brain inflammatory responses mediated by proinflammatory agents.
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PMID:Peptide modulation of inflammatory processes within the brain. 973 Jun 84

The intravascular enhancement (IVE) sign, also known as the "arterial enhancement sign", is an abnormal finding in the brain on contrast-enhanced MRI studies. IVE has been described in arterial cerebrovascular disorders, most commonly in acute or subacute arterial ischemic infarcts. However, the specificity of this sign has not been established. We describe four patients with disorders other than arterial strokes in whom gadolinium-enhanced high-field (1.5 T) MRI suggested IVE. The conditions were herpes simplex viral encephalitis, idiopathic cerebellitis, pneumococcal meningitis, and superior sagittal sinus thrombosis with venous infarction. IVE in these cases may be due to multiple factors, including arterial, venous, perivascular, and leptomeningeal or sulcal contrast medium accumulation. Our observations suggest that arterial ischemia, previously described as the cardinal cause of IVE, probably does not explain all instances, and urge caution in interpreting this sign as a specific MRI manifestation of acute arterial infarction or ischemia.
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PMID:The cerebral intravascular enhancement sign is not specific: a contrast-enhanced MRI study. 1009 May 99


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